VTE Flashcards
which is the only factor not generated by the liver
factor 8
where is factor 8 synthesized
by vascular endothelial wall and released into the blood stream
what happens to factor 8 in the bloodstream
cleaves into 2 separate components
- factor 8C coagulant material which goes to the intrinsic pathway of fibrin
- factor 8 vWF factor which is used in the formation of platelets
what does thromboaxane A2 do
platelet aggregator
vasiconstrictor
how is TXA2 formed
in platelets cox enzyme converts arachodonic acid to thromboxane a2
what do prostacyclins do
platelet anti-aggregator
vasodilator
how are prostacyclins formed
in the blood vessel wall AA converted by COX to PGI
what 3 things are produced by platelets
TXA2
serotonin
adp
what does the GPIIb/IIIa receptor complex do
binds to fibrinogen and brings platelets together
what causes platelet activation
TXA2, thrombin, collagen
increased cystolic calcium
what happens at the GPIb/IX receptor
vWF binds and adheres the platelet against the wall of collagen
factors predisposing to bleeding
open vessel
platelet defects
pro clotting factor deficiences
what is added to the test tube of patient plasma for prothrombin time
thromboplastin and calcium
more than ___ seconds is suggestive of a defective ______ pathways in prothrombin time
greater than 12 seconds
defective extrinsic and common
prothrombin time is sensitive to reductions in which factors
1, 2, 10, 7
warfarin reduces the synthesis of which factors
2, 7, 9 , 10
which factor has the short half life**
factor 7
why might a thrombotic state still be present even after you see an increased prothrombin time right after initiating warfarin
factor 7(extrinsic) very short half life so will decrease the PT right away still some facotr 2 or 10 around and can be activated by the intrinsic pathway (not measured by PT)
INR and aPPT are not altered by _____ (4)
thrombocytopenia
defective platelets
ASA
NSAIDS
INR and aPPT are prolonged when
fibrinogen level is low
what is added to the patients plasma in the aPPT test
activating agent (mimics collagen exposure) calcium
> _____ suggestive of a defective _____ in aPTT
> 30seconds
defective intrinsic and common
aPPT test is sensitive to reductions in which factors
1,2,10 (common)
9,11,12 (intrinsic)
heparin moa
immediately accelerates the binding of antithrombin 3 to activated forms of factors 2,9,10,11,12 thus inactivating them
when are heparin effects seen in aPPT
immediate
max effects after 6 hours (4.5 half lives of heparin)
relationship between inr and PT
thromboplastins different in different contries do get different prothrombin times
INR is standardized throughout every country using the PT and the international sensitivity index
INR formular
PT(patient)/PTc(mean time for your lab control) ^ISI (international sensitivity index)
whats the normal INR range
0.9-1.1
treated patients: 2-3
what are white thrombi
arterial thrombi
primarely made of platelets
ex. coronary artery thrombosis - stroke
what are red thrombi
venous thrombi
primarily fibrin and RBC and a small platelet plug
ex, deep vein thrombi - on a plane
what is th ehemostatic balance
balance between clotting (procoagulants) and bleeding (anticoagulants)
what is type A hemophilia
which test would it show up in
deficiency of factor 8C, but normal8vWF “classical”
aPPT test
what is type B hemophilia
deficiency of factor 9 “christmas disease”
what is von willebrands disease
diminished factor 8 VWF but normal facotr 8
what is disseminated intravascular coagulation
simultaneous clotting and bleeding
commonly seen with severe sepsis
what happens with clotting factors and anticoagulants in severe liver disease
factor deficiencies cause bleeding - decresed hepatic synthesis of factors 1-13 except 8
also decreased synthesis of antithrombin, plasminogen and alpha 2 antiplasmin
have anti and pro coagulant imbalances so can clot or bleed
DIC may also occur
what is thrombocytoopenia
decreased platelet count from either a decrease in bone marrow production(gradual) or due to increased peripheral destruction (more rapid)
what is heparin induced thrombocytopenia
allergic reaction to heparin
platelets fall 5-10 days after becoming prothrombic
name 3 thrombogenic risk factors
obesity over 40 yoa malignancy immbolization major surgery acute MI multiple trauma
unfractionated heparin will not work if have a deficiency in what
antithrombin 3
LMWH examples and mechanism
enoxaparin,dalteparin, tinzaparin
binding wiht antithrombin 3 and neutralizes activated forms of 10a
why does warfarin initially increase clotting
depletes the synthesis of protein C - a anticoagulant
dont give alone for the first few days
how do asa/nsaids work
inhibit TXA2 syntheiss by acetylating COX thereby decreasing platelet aggregability
tenecteplase moa
thrombolytic (dissolves clots)
increased fibrinolysis
converts plasminogen to plasmin
desmopressin moa
increased release of factor 8-vWF thus enhancing platelet aggregability
pro platelet aggregation
bivalirudin and argatroban inhibition
factor 2a inhibitor
dabigatran inhibition
factor 2a inhibitor
rivaroxaban, fondaparinux, apixaban inhibition
factor 10a inhibitor
deep vein thrombosis signs and symptoms
unilateral
warm swollen
painful
starts in calf then moves up to femoral positive homans sign
what is the homans sign
pain upon dorsiflexion of the foot
clinical presentation of pulmonary embolism
tachypnea (rapid breathing)
chest pain
dyspnea
tachycardia
test performed in pulmonary embolism and why
chest xray
ekg
blood gases
used to rule out other causes of symptoms, all should be negative
based on the chads score what drugs should be used
0 = asa only 1 = asa OR DOAC or warfarin >2 = DOAC or warfarin
DOACs recommended for all forms of non valvular afib and what valvular forms
mitral regurgitation
aortic stenosis
aortic regurgitation
do not use doac (direct oral anticoagulant) in which conditions
mitral stenosis
prosthetic vlave disease
patients with prosthetic heart valves are at increeased risk of what
developing valvular thromboembolism
warfarin inr target of ___ for valves in aortic position and no risk factors for thromboembolism
2.5 (2-3)
warfarin INR target of ____ for patients with valves in the nitral position and risk factors for thromboembolism
3 (2.5-3.5)
drug recommendations for bioprosthetic valves
lower risk for systemic embolization
assa 75-100mg
for the first 3-6 months after bioprosthetic vlavue surgery warfarin inr of 2.5 (2-3)
when to check aptt and platelets when on heparin
check aPTT every 6 hours initially and adjust to maintain desired range within first 24 hours
check platelet count daily
when should tou stat warfarin and stop heparin for coagulation disorders
start warfarin mg day 1 and adjust according to INR goal
stop heparin after at least 5 days of combined therapy and when INR is greater than target for at least 2 consecutive days
starting and stopping for heparin and warfarin in patients with a major pulmonary embolism or iliofemoral vein thrombosis
run heparin for up to 10 days and start warfarin after a delay of 4 days
parameters to monitor for therapy for UFH,LMWH, or warfarin
aptt inr hbg platelets clinical signs of bleeding
critical signs of bleeding*****
melena (blood in stool) hematuria (blood in urine) ecchymosis (severe bleeding) hematemesis (vomiting blood) hemoptysis (coughing blood) epistaxis (bleeding from nose) at least daily
when would you use thrombolytic therapy for DVT/PE
pulmonary embolism with shock
massive dvt with limb gangrene
why dont you just give lots of vit k to reverse warfarin effects for surgery
will take over a week for warfarin to work again
if try to reach inr after by increasing warfarin when the vit k wears off the inr will skyrocket
for provoked vte how long and what target of warfarin
warfarin for 3 months
inr target 2.5
for idiopathic vte how long should you use warfarin
more then 3 months
up to 2.5 years
if a patient has thrombotic recurrence despite anticoagulation how should you continue warfarin
warfarin indefinately
inr target 3
when else should you continue warfarin indefinitely
patient has risk factors malignancy AT deficiency previous thromboembolism LV dysfunction ???
which drugs should you avoid in patients with CrCl <30
LMWH
dabigatran
rivaroxaban
apixaban
drug interactions with dabigatran *
inhibitors/inducers of p-gp
ex. amidarone, azithromycin, carvediol, diltiazem
drug interactions of rivaroxaban and apixaban
inhibitors/inducers of p-gp and cyp 3A4
drug interactions of LMWH
none known
reversal agents for anticoagulant related bleeding – effectivenss is anticoagulant specific
protamine iv
bit k
fresh frozen plasma
recombinant factor VIIa (increased risk of thrombosis)
4 factor prothrombin complex concentrates
which reversal agents arent really recommended for warfarin bleeding
rFVIIa
4-PCC
dialysis not effective in overdose
what is idarucizuman
monoclonal antibody fragment specifically targeted at dabigatran
when should you stop warfarin before surgery
1 week before surgery
what is warfarin used to treat
major thrombosis
time for full effects of warfarin
more than a week
can you use warfarin in renal impairmetn
yup
what is dabigatran rivaroxaban and apixaban used to prevent
stroke with a fib
onset of dabigatran
1 hour full effects in 3 days
when should you stop dabigatran, rivaroxabin, apixaban before surgery
1-2 days before
what is effective and not effective for reversal in dabigatran
hemodialysis
rFVIIa
5g idarucizumab 1st line
not FFP or 4-PCC
why isnt ffp used for dabigatran reversal
provides anticoagulation by inhibition not by depleting clotting factors
what value does dabigatran increase
aPPT test
not recommended for monitoring
which reversal agents are and arent effectiv ein rivaroxabin and apixaban
use 4-PCC
not dialysis or FFP
whats a greenfield filter
mechanical device in the inferior vena cave to filter emboli originating from lower extremities
who might be considered for green field filter
contraindication to anticoagulant theray
recurent pulmonary embolism despite anticoagulation
counselling for LMWH, warfarin, DOACs
inform doctors and dentists of use
avoid asa and other nsaids
discuss new drugs or otc becuase many interactions
maintain normal diet despite vit k
medic alert bracelet
inr monitoring to ensure adequate coagulation
inform doctor promptly if clinical signs of bleeding
